ATALAY, M., D. E. LAAKSONEN, S. KHANNA, E. KALISTE-KORHONEN, O. HÄNNINEN, and C. K. SEN. Vitamin E regulates changes in tissue antioxidants induced by fish oil and acute exercise. Med. Sci. Sports Exerc., Vol. 32, No. 3, pp. 601–607, 2000.
Prooxidant effects of fish oil supplementation could unfavorably affect the cardiovascular benefits of fish oil. We tested the effects of 8 wk vitamin E cosupplementation with fish oil on antioxidant defenses at rest and in response to exhaustive exercise in rats.
Rats (N = 80) were divided into fish oil, fish oil and vitamin E (FOVE), soy oil, and soy oil and vitamin E (SOVE) supplemented groups. For the vitamin E supplemented rats, corresponding groups (FOVE-Ex and SOVE-Ex) performed an acute bout of exhaustive exercise after the supplementation period.
Fish oil supplementation increased the activity of catalase, glutathione peroxidase, and glutathione-S-transferase in the liver and red gastrocnemius (RG) muscle. Fish oil decreased liver total glutathione (TGSH) levels. Vitamin E supplementation decreased antioxidant enzyme activities to levels at or near those in SOVE in a tissue specific pattern. Vitamin E increased TGSH in liver, heart, and RG. Regression analysis showed TGSH to be a negative determinant of protein oxidative damage as measured by protein carbonyl levels in both liver and RG. Catalase activity was associated with liver lipid peroxidation as measured by thiobarbituric acid–reacting substances. The exercise-induced decrease in hepatic TGSH tended to be less in FOVE versus SOVE. Exhaustive exercise also modulated tissue antioxidant enzymes.
Vitamin E supplementation markedly decreased fish oil induced antioxidant enzyme activities in all tissues. Sparing of glutathione may be an important mechanism by which vitamin E decreased tissue protein oxidative damage.
Department of Physiology and National Laboratory Animal Center University of Kuopio, 70211 Kuopio, FINLAND; and Lawrence Berkeley National Laboratory/EETD University of California at Berkeley, Berkeley, CA 94720-3200
Submitted for publication November 1998.
Accepted for publication June 1999.
Address for correspondence: Chandan K. Sen, Ph.D., Biological Technologies, Lawrence Berkeley National Laboratory/EETD, One Cyclotron Road, Building 90, Room 3031, Mail Stop 3200, University of California, Berkeley, CA 94720-3200. E-mail: cksen@socrates. berkeley.edu.